http://scan3.home.mindspring.com/id11.htmlEnhancingOutcome of Hyperbaric Oxygen TherapyDenis Scannell DMT

Many visitorshave asked more information about optimal number of sessions and types of additional therapy to maximize benefits.These are mere guidelines. Every patient is different, and therapy must be tailored to him/her.During the last 5 years it has become clear that hyperbaric oxygen for treatment of medical illness is beneficial at pressures as low as 1.3-1.5 ATA, which decreases the risks of oxygen toxicity to a minimum.But, though extremely safe when used properly, a mild hyperbaric chamber doesn't increase the concentration of oxygen diffused in body water enough to achieve the best results.Oxygen by mask at more thanfive liters per minute is also necessary. ISCHEMIC STROKE: A minimum of ten 90 min sessions. Serial neurological exams done by a trained professional and bio-feedback may beadditional help. Keep in mind that there are a number of neurological scores and the rehabilitation expert must be familiar with them. BRAIN INJURY: As above. Up to 50 treatments may be necessary. SPINE INJURY: Early treatment decreases swelling and inflammation. Severance of nervous channels cannot be reversed by hyperbaric oxygen. MULTIPLE SCLEROSIS: Studies done inEnglandsuggest that early treatment of MS with hyperbaric oxygen is beneficial in slowing down the progression of the disease. Patients who underwent 50 sessions with weekly "maintenance" therapy had a better neurological function for many years than patients who did not receive hyperbaric oxygen. NON-HEALING WOUNDS, ENHANCEMENT OF WOUND HEALING: Post-operative wounds and chronic wounds heal well, and after about 10 sessions there is new, permanent capillary growth. STATUS POST PLASTIC SURGERY:We recommend 2 preoperative sessions of 90 min and 5 postoperative daily sessions. Used by many plastic facial surgeons. OSTEORADIONECROSIS: 10-20 daily treatments at 1.3 ATA are as good as 3 ATA and there are no risks of oxygen toxicity. DIABETIC ULCERS: New capillary growth to the lower extremities starts at 10 treatments. Chronic ulcers heal.Improvement of diabetic neuropathy. Must follow scrupulous visual monitoring of lower extremities. AUTOIMMUNE DISEASES SCLERODERMA, RHEUMATOID ARTHRITIS, CROHNS' DISEASE,ULCERATIVE COLITIS:Hyperbaric oxygenSTOPSautoimmunity. Recently also used for eczema with weeping wounds and open sores.For CUC, pain and bleeding improved after 15 sessions, andfrequency of bowel movements returned to 1-2 a day at30 sessions. Liver enzymes were cut by 1/3, stool leukocytes drastically decreased. FIBROMYALGIA: Stiffness, swelling of the lower extremities improves after 10 sessions, but it requires 20 or more to begin feeling normal. CHRONIC FATIGUE:Depression improves after as little as 3 sessions. This condition is chronic and requiresdaily sessions for months. AUTISM:We have treated three autistic children and confirmour colleagues reports. Treatments require over sixty daily sessions, butresults are encouraging.

http://scan3.home.mindspring.com/id14.htmlA:THE EFFECT OF HYPERBARIC OXYGEN ON SCLERODERMABackground:Scleroderma is an autoimmune condition in whichcollagen deposits in abnormally high concentration in the subcutaneous tissue and other areas of the body. In some cases, this restricts blood supply to the skin and prevents normal wound healing. Wounds fester and become infected, decreasing oxygen delivery even further. Hyperbaric oxygendelivers oxygen to ischemic, marginal wounds andis known to accelerate wound healing by as much as 50%. Additionally, hyperbaric oxygen is an immunomodulator, which decreases the production of ICAM and Tumor Necrosis Factor alpha by vascular endothelial cells and neutrophils (Refs 1,2,3,4,5).Study Design:A 50 year-old white female ceramic artist with diffuse scleroderma for 10 years was referred to our Institution for evaluation of more than 10 open wounds in both her upper extremities, present for at least 6 months, and refractory to every conventional therapy.A 46 year-old white male trumpet player with cutaneous scleroderma for 7 years was referred to our Institution for symptoms of Raynaud and ulcers on his fingertips lasting the entire winter season, associated with numbnessin his fingers on both hands.Each patient was given 50 consecutive 90 min. sessions of Hyperbaric Oxygen with a mild hyperbaric chamber at 1.3 ATA.Results:In both cases, initial oxygen saturation readings were not obtainable in any of the fingers, which were pale and insensate. Both patients had 5 to 10 episodes of Raynaud per day. No change was observed during the first 10 treatments. After the 20th, it was observed that the episodes of Raynaud, which had been decreasing, had completely abated. Oxygen saturation readings became obtainable and improved slowly. At 30 treatments, both patients showed definite evidence of healing their wounds. Additionally, sensation returned to the tip of their fingers. At 40 treatments, their pulse oximetry readings were consistently 98% in all fingers, and there was a dramatic progress in wound healing. Therapy was stopped at 50 sessions. Approximately a year after hyperbaric oxygen therapy was discontinued, wounds remained healed and pulse oximetry readings continued to be 98%, suggesting that new capillary growth had been permanently achieved. New wounds did not get infected and healed rapidly. Though before their treatments, both patients had experienced a slow progression of their disease, no new symptoms had appeared. In fact, there appeared to be a regression in the amount of deposited collagen.Conclusions:Although scleroderma is not an approved indication for hyperbaric oxygen therapy, the ischemia it causes can be combated by hyperbaric oxygen. The diffusion of oxygen inareas of the body,ischemic because of scleroderma, may change thenumber and distribution of capillaries in these areas, thus allowing healing. Additionally, hyperbaric oxygen may ameliorate this debilitating chronic autoimmune condition.References:1. Buras JA, Stahl GL, Svoboda KK, Reenstra WR. Hyperbaric oxygen downregulates ICAM-1 expression induced by hypoxia and hypoglycemia: the role of NOS. Am. J. Cell. Physiol. 2000 Feb;278(2):C292-302.2. Hong JP, Kwon H, Chung YK, Jung SH. The effect of hyperbaric oxygen on ischemia-reperfusion injury: an experimental study in a rat musculocutaneous flap. Ann. Plast. Surg. 2003 Nov;51(5):478-487.3. Yamashita M, Yamashita M. Hyperbaric oxygen treatment attenuates cytokine induction after massive hemorrhage. Am. J. Physiol. Endocrinol. Metab. 278:E811-E816, 2000.4. Wallace DJ, Silverman S, Goldstein J, Hughes D. Use of hyperbaric oxygen in rheumatic diseases: case report and critical analysis. Lupus1995 Jun;4(3):172-175.5. Thom SR, Mendiguren I, Hardy K, et al. Inhibition of human neutrophil beta2 integrin-dependent adherence by hyperbaric O2. Am J Physiol. 1997;272(3 Pt 1):C770-777.B:ACCELERATING STROKE RECOVERY WITH HYPERBARIC OXYGEN THERAPY (HBO)Background:Ischemic stroke is common, debilitating, and disruptive. Recent advances in medical therapy have reduced mortality, but complete recovery, though frequent, may take weeks or, more commonly, months. HBO, though not an approved therapeutic modality, has been known to increase rate of wound healing by as much as 50%. We tested the hypothesis that the same could be true for ischemic strokes.Study Design:Three patientswith recent ischemic strokes were entered in this study. Another two patientswith similar symptoms could not, or would not receive HBO and were followed clinically. The times of all strokesvaried between 8 and 32 days. Disabilities ranged from hemianopsia to unilateral lower extremity weakness. All patients complained of short term memory loss, difficulty in maintaining concentration and disorientation.Patients underwent 20 consecutive daily sessions of HBO at 1.3 ATA for 90 min. or no HBO therapy.Results:In the HBO group, no benefit was seen for the first 10 sessions. At times varying between the 12th and 15th session, disorientation and confusion lifted,with return to clear decision-making andactive participation in theirphysical rehabilitation.After the 20th session, field of vision demonstrated a15 and 25% improvement (2 patients), motorstrength was improved (1 patient), sense of well-being had returned in all patients.Symptoms of disorientation and weakness were still present in both non-HBO patients two months after their stroke, though they had some return of their muscular tone.Conclusions:Though HBO in the proper dose, in the face of an acute stroke, is as effective astPA, (1) itcannot recover neurons after they have died. However, it may accelerate the speed of recovery, possiblyby decreasingcerebral edema (2)and inducing growth of new capillaries.References:1. Boer KM, Boer RC Jr, Strauss MB, Jimenez A, Minkiewitz KM. Hyperbaric oxygen therapy for acute ischemic stroke. Undersea Hyperb Med. 1998;5(suppl):13.Abstract.2. Pearson RR, Goad RF. Delayed cerebral edema complicating cerebral arterial gas embolism: case histories. Undersea Biomed Res. 1982;9;283-296.Other stroke references:1. Nighoghossian N, Trouillas P, Adeleine P, Salord F. Hyperbaric oxygen in the treatment of acute ischemic stroke: a double-blind pilot study. Stroke. 1995;26:1369-1372.2. Rogatsky GG, Shifrin EG, Mayevsky A. Optimal dosing as a necessary condition for the efficacy of hyperbaric oxygen therapy in acute ischemic stroke: a critical review. Neurol Research. 2003;25:95-98.3. Holbach KH, Caroli A, Wassmann H. Cerebral energy metabolism in patients with brain lesions in normo- and hyperbaric oxygen pressures. J Neurol. 1977;217-17-30.4. Thom SR. Antagonism of carbon dioxide-mediated brain lipid peroxidation by hyperbaric oxygen. toxicol Appl Pharmacol. 1990;105:340-344.5. Ronning OM, Guldvog B. Should stroke victims routinely receive supplemental oxygen? A quasi-randomized controlled trial. Stroke. 1999;30:2033-2037.6. Anderson DC, Bottini AG, Jagiella WM, et al. A pilot study of hyperbaric oxygen in the treatment of human stroke. Stroke. 1991;22:1137-1142.C:ULCERATIVE COLITIS: IN REMISSION WITH HYPERBARIC OXYGEN.TWO CASE REPORTSBackground:Ulcerative colitis (UC)affects 1.2 million people in theUSA, mostly teen-agers to young adults. It is a disease in which the last 3 feet of our bowel, the colon, lose their inner layer, the mucosa. Inflammation, or cryptitis, of the buddingportion of the mucosa, is a hallmark of the disease. Mayor complications are sclerosing cholangitis, which leads to liver failure necessitating transplant, and colon cancer. Its cause is unknown.Hyperbaric oxygen, by decreasing inflammation and promoting healing, could improve this condition.Case Report:Two white males,30 and 27year-old, diagnosed with UC three and seven years prior totheir hyperbaric treatment, were referred to our Center.They had failedeverytherapy, and were on 40 mg of prednisone or 30 mg of 5MPa day. In spite of it, they were having 7-9 bloody bowel movements a day, and were home-confined, disabled, not being able to maintain employment. Theyunderwent 45 to 65sessions of HBO at 1.3 ATA, 120 min twice a day, intheir own home.Results:In both patients, no improvement was seen for the first 15 sessions. By the 20th, bleeding subsided. By the 30th, the number of bowel movements was reduced to 2 per day. By the 40th, the stool was solid, without blood. Patients' stool leukocyte count (2,3)was improved (3-5/hpf), suggesting decreased inflammation. In the patient on prednisone, liver function tests revealed a 35% decrease in alkaline phosphatase (280 to 182) suggesting an improvement of his sclerosing cholangitis.Both patients could leave their house for the first time in years, and return to work. Both are off steroid and antimetabolitic drugs.Conclusions:Mild HBO is effective in the treatment of Ulcerative Colitis. Inflammation is reduced, or,as in our cases, truncated.Crohn's Colitis Patient's testimony.S.G., 57 years old male reports regarding his experience with HBOT in treating his Crohn's Disease.'As you know, I used the Vitaeris 320 in my home over a two month period, totaling 80 sessions averaging 1 & 1/2 hours each. When I began HBOT treatment, I had also just started a course of drug therapy (prednisone and metronidazole) to arrest a flare. After 5 weeks of HBOT and at the conclusion of tapering off of the prednisone, I felt better than I had in a long time. However, just a few days later, I began to experience the early symptoms of another flare. At that point I had been using the chamber in a "maintenance" mode, three or four so (90 min.) sessions every week. At the onset of the flare, I increased the chamber sessions to two a day for a week and was able to successfully arrest the flare without the introduction of steroids. This was a significant achievement and I felt validated the efficacy of HBOT in treating my flare symptoms.Since purchasing a chamber, I have been using it, on average, four sessions/week and maintaining a fairly good level of health, with occasional periods of disruption. Overall, I'm pleased with the chamber and expect to continue to incorporate it into my course of treatment.'Received 5/17/2007.References:1. Logan R.Inflammatory bowel disease incidence: up, down or unchanged?Gut. 1998, March;42:309-311.2. Silberer H, Kuppers B, Mickisch O, Baniewicz W, Drescher M, Traber L, Kempf A, Schmidt-Gayk H. Fecal leukocyte proteins in inflammatory bowel disease and irritable bowel syndrome.Clin Lab.2005;51(3-4):117-126.3. Hanauer S. Update on the Etiology, Pathogenesis and Diagnosis of Ulcerative Colitis. Nat Clin Pract GastroenterolHepatol.2004;1(1):26-31.D:RESOLUTION OF LYME DISEASEWITH HYPERBARIC OXYGEN THERAPY (HBO)Background:Lyme disease affects two hundred thousand people a year in theUnited States. Diagnosis is frequently delayed and treatmentcomplex, involving years of therapy.Though rarely life-threatening, it constantly interferes with daily life.Study Design:A twenty-four year old woman, diagnosed with Lyme disease a year prior, but symptomatic for more than three, was referred to our clinic for treatment. She slept four hours a night, was weak and listless, couldn't hold a job, and had severe joint and muscle pains.After a thorough history and physical exam, she was cleared for hyperbarictreatment. Aminimum of 40, 120 min. treatment were administered. The patient never received antibiotics, or any other treatment.Results:Benefit was seen almost immediately. By the tenth session, the patient was sleeping a full night sleep, and the joint and muscle pains had subsided completely. Activity level increased steadily, as well as her well being.Conclusions:HBO may be effective in the treatment of Lyme disease in selected patients.E:EARLYMULTIPLE SCLEROSIS (MS) CANBE STALLED WITH HYPERBARIC OXYGEN THERAPY (HBO)Background:Multiple sclerosis (1) is a progressive, debilitating autoimmune disease in which the myelin of peripheral nerves is destroyed. It has periods of relative quiescence alternated withreactivation. Though HBO has been used and researched with this disease (2), controversy exists about its benefit. We propose the hypothesis that, because loss of nerve function leads to disappearance of neuromuscular plaques and consequent loss of musculature, early treatment, within 1 year of diagnosis, has the best chance of success. We further propose that, since HBOdiminishes inflammation and levels of inflammatory mediators, discontinuation of HBO may lead toreturn ofprogression of the disease.Study Design:Three female patients with MS age 42, 48 and 53 were diagnosed with MS 3 to 12 months prior to HBO therapy. Symptoms ranged from transientdifficulty focusing to intermittent weakness of their upper extremities, toinability to control bladderfunction and didn't improve with traditional medical therapy. Each underwent 42-60, 120 min. dailysessions with complete resolution of their symptoms.Two patients continued daily therapy to 100 and 120 sessions, then tapered down to 2 weekly sessions,without return of symptoms.One patient interrupted her therapy at 49 sessions, and felt well.Results:At 1 year, symptomshad not returned in the treated patients, but did in the third,who had stopped therapy.Conclusions:This small study suggests thatwith thorough patient selection andadequate therapy, HBO may be beneficial in patients with early MS.F:CHRONIC SYMPATHETIC DYSTROPHY: A TREATABLE DEBILITATING DISEASE. CASE REPORTSympathetic dystrophy starts innocently: a sprained ankle, a toe infection, a torn ligament, but the pain doesn't end, even when the injury has healed. It continues, and migrates upward, jumps to the unaffected limb. As a result, the sufferer is relegated to bed, treated with pain medications.We report a case of a teenage girl who didn't respond well to conventional therapy, but began to feel better after 20 sessions of HBO at 2 ATA, and had remarkable results after another 20. But her life was upside down with daily travel. A trial of 20 sessions in a mild hyperbaric chamber convinced her that she could live symptoms free at home with their own chamber. To this date, she has responded as well to daily 2-hour sessions in a mild (1.3 ATA)hyperbaric oxygenchamber, and her symptoms have not returned.

http://www.healing-arts.org/children/hyperbaric.htmInformation About Using HBOT for Auto-immune diseases1.Anton'ev, A.A. and Nomnoeva, T.N. [Use of hyperbaric oxygenation in dermatology] Primenenie giperbaricheskoi oksigenatsii v dermatologii. Vestn.Dermatol.Venerol. (2):27-31, 1986.2.Dowling, G.B., Copeman, P.W., and Ashfield, R. Raynaud's phenomenon in scleroderma treated with hyperbaric oxygen. Proc.R.Soc.Med. 60(12):1268-1269, 1967. Notes : 0035-9157 English England Journal-Article 68090745 6803.3.Lukich, V.L., Grebenev, A.L., Matrenitskaia, N.A., and Grabskii, M.A. [Treatment problems in systemic scleroderma using hyperbaric oxygenation] Problemy lecheniia sistemnoi sklerodermii giperbaricheskoi oksigenatsiei. Klin.Med.Mosk. 62(3):26-31, 1984.4.Iakunin, G.A., Grebenev, A.L., Lukich, V.L., Smolianitskii, A.I., and Grabskii, M.A. [Rheological and coagulative blood properties in patients with systemic scleroderma undergoing hyperbaric oxygenation in combined treatment] Sostoianie reologicheskikh i koaguliatsionnykh svoistv krovi u bol'nykh sistemnoi sklerodermiei pri primenenii giperbaricheskoi oksigenatsii v kompleksnom lechenii. Ter.Arkh. 55(7):120-124, 1983. Notes : 0040-3660 Russian; Non-English USSR Journal-Article 0 84018192 8401.5.Lukich, V.L., Kurakina, L.V., and Poliakova, L.V. [The role of hyperbaric oxygenation in the treatment of systemic diseases] Rol' giperbaricheskoi oksigenatsii v lechenii sistemnykh zabolevanii. Klin.Med.Mosk. 69(7):15-20, 1991. Notes : 0023-2149 Russian; Non-English USSR Journal-Article; Review; Review-Tutorial 92047220 9202.6.Wallace, D.J., Silverman, S., Goldstein, J., and Hughes, D. Use of hyperbaric oxygen in rheumatic diseases: case report and critical analysis. Lupus. 4(3):172-175, 1995. Notes : Department of Medicine, Cedars-SinaiMedical Centre, Los Angeles, CA, USA 0961-2033 English EnglandHyperbaric oxygen has been used in patients with rheumatic disease for many years without reports of untoward or unusual complications for a variety of non-rheumatic indications. Recent evidence that hyperbaric oxygen inhibits the actions of certain cytokines, acts as an immune modulator and may help cognitive dysfunction has resulted in a re-examination of its potential role in rheumatic diseases. A case report of a lupus scleroderma crossover patient is presented whose cognitive dysfunction improved after hyperbaric oxygen therapy. The history of hyperbaric oxygen and its physiology are related, along with a focused review of its effects on the immune and central nervous systems.7.Makeeva, N.P., Balakhonova, N.P., Kurakina, L.V., and Kamshilina, L.S. [Microcirculation in patients with systemic scleroderma during treatment using hyperbaric oxygenation] Mikrotsirkuliatsiia u bo'lnykh sistemnoi sklerodermiei pri lechenii metodom giperbaricheskoi oksigenatsii. Klin.Med.Mosk. 67(6):107-109, 1989. Notes : 0023-2149 RussianHyperbaric oxygenation treatment of systemic scleroderma has a favorable effect on microcirculatory changes whose positive dynamics can be demonstrated by conjunctival biomicroscopy. These changes include accelerated blood flow and decrease in the degree of erythrocyte aggregation. The method can be used or the objective assessment and for prognosis of the effectiveness of hyperbaric oxygenation treatment in patients with systemic scleroderma.

http://www.whitakerwellness.com/our-therapies/hyperbaric-oxygen-therapy.htmlHyperbaric oxygen therapy (HBOT) is medicine's most efficient method of transporting oxygen to cells throughout the body. When you breathe oxygen at normal atmospheric pressure, it is transported on the hemoglobin in your red blood cells. Under pressure, however, oxygen dissolves in the plasma, cerebrospinal fluid in the brain and spinal cord, lymph, and other body fluids. It is therefore easily delivered to all tissues, and even areas with limited blood flow are afforded the tremendous healing benefits of oxygen.

HBOT also curbs infection, by providing a hostile environment to anaerobic bacteria, which thrive in the absence of oxygen. It promotes the growth of new capillaries and blood vessels to areas with poor circulation for cardiovascular support and boosts collagen formation for faster wound healing. It also mobilizes rejuvenating stem cells. Studies show that after just one HBOT treatment, concentrations of circulating stem cells doubled, and after a full course, there was an eight-fold increase. The end result is dramatic benefits forstroke, head and spinal cord injuries,diabeticulcers, slow-healing wounds, burns,autism, and a broad range of other conditions.

A typical HBOT session lasts 45 minutes to two hours. During this time, you sit or recline comfortably in a pressurized chamber while breathing 100 percent oxygen through a mask. You can listen to music, read, watch a movie, or simply relax. As the chamber is pressurized, you may notice increased pressure in your earsa feeling similar to that of a flight landingbut there is no other discomfort. When the session ends, the pressure is slowly returned to normal. Hyperbaric treatments are repeated, depending on the condition, anywhere from five to 40 times. Therefore, we encourage patients interested in HBOT to enroll in ourBack to Health Program.In conventional medicine, HBOT is primarily used to treat decompression illness (the bends), carbon monoxide poisoning, necrotizing wounds, and other acute conditions. At Whitaker Wellness, we use this invaluable therapy for a far broader range of health challenges.

HBOT, combined with physical rehabilitation, is the best therapy available for patients who have suffered a stroke. When the body and brain are infused with massive amounts of oxygen during hyperbaric treatment, damaged cells literally wake up. This, plus the HBOT-stimulated growth of new blood vessels and the increase in circulating stem cells, provides tremendous benefits for our patients.Strokepatients once given little hope are mobile and active again.

Thanks to HBOT treatment, individuals scheduled for limb amputation due to gangrenousdiabeticulcers have cancelled surgeries and are walking around on their own two feet. Patients withParkinson's diseaseandautismmake dramatic strides. And people with serious burns, head or spinal cord trauma, and other injuriesas well as those who have had plastic surgery or other interventionsheal much more rapidly and get back on the road to normal function much earlier than anticipated.

The beauty of hyperbaric oxygen therapy is that it works synergistically with the otherinnovative therapiesand nutritional supplement protocols your Whitaker Wellness physician will prescribe for you. The end result is often reduction or elimination of prescription drugs and enduring improvements in overall health.Conditions that may benefit from the multiple healing mechanisms of hyperbaric oxygen therapy include: Autism Bacterial infections of the skin Burns Carbon monoxide poisoning Decompression sickness ("the bends") Diabetic ulcers and other complications Head and spinal cord injuries Infections Migraines Multiple sclerosis and other autoimmune diseases Musculoskeletal injuries Neurodegenerative disorders Non-healing wounds Parkinson's disease Post-surgical healing Spider bites Stroke

http://www.hyperbaricoxygentherapies.com/hyperbaric-oxygen-rheumatic-diseases.phpOccasional ReviewUse of Hyperbaric Oxygen in Rheumatic Diseases: And Critical AnalysisD.J. Wallace 1,2 S. Silverman.2* J.Goldstein 3,and D. Hughes 41Department of Medicine Cedar-Sinai Medical Center 2UCLA School of Medicine, Los Angeles, CA. 3 The Chronic Fatigue Syndrome Institute. Anaheim CA. And 4 The Hyperbaric Oxygen Institute, San Bernardino, CA USAHyperbaric Oxygen has been used in patients with rheumatic disease for many years with out reports of untoward or unusual complications for a variety of non-rheumatic indications. Recent evidence that hyperbaric oxygen inhibits the actions of certain cyctokins, acts as an immune doculator, and might help cognitive dysfunction has resulted in a re-examination of its potential role in rheumatic diseases. A case report of a LUPUS/ Scleroderma crossover patient is presented whose cognitive dysfunction improved after hyperbaric oxygen therapy. The history of hyperbaric oxygen and its physiology are related, along with a focused review of its effects on the immune and central nervous systems. Areas which might warrant further consideration by rheumatologists are outlined, as well as areas of concern.

Keywords: hyperbaric oxygen: Scleroderma: rheumatic Diseases

Introduction:

Hyperbaric Oxygen Therapy is defined as the subjecting of patients to pure oxygen breathing at ambient temperatures, which are greater than normal atmospheric pressure.Although concepts of hyperbaric oxygen therapy were first employed in 1662, its modern use other than for decompression dates from 1956, when hyperbaric oxygen was used to perform cardiac surgery in Holland 1. Mechanically, the most common applications of hyperbaric oxygen are to dissolve air or gas emboli and treat divers with "bends" or decompression illness.

New insights into the biochemical and immune interactions of hyperbaric oxygen have increased interest in its potential applications over the past decade. The United States Medicare System has approved hyperbaric oxygen for 13 indications ranging from acute carbon monoxide intoxications, gas gangrene, and osteroradionecroisis to acute arteriolar insufficiency. Over the last 20 years, patients with a variety of conditions, especially multiple sclerosis, have reported cognitive improvement after undergoing hyperbaric oxygen. One lupus/ scleroderma crossover patient, whose case is reported here, underwent hyperbaric oxygen therapy specifically for cognitive impairment and experienced subjective and objective improvements. Her case is presented and our concepts of hyperbaric oxygen and the immune and central systems are reviewed.

Case Report:

A 53-year-old caucasian woman was a flight attendant in an usual state of health in 1979 when she underwent a thyroidectomy and inadvertent parathyroidectomy for Graves disease. In February 1980, her Heyer Schulte saline breast implants (placed in 1977 for cosmetic purposes) were replaced with Cox-Uphoff Silicone prostheses. She was well until 1986, when she presented to UCLA Medical Center with subcutaneous arthritis, Raynaud's phenomenon, Sclerodactyly, inflammatory arthritis, and erythermatous rashes. A work-up demonstrated an ANA of 1:40 (speckled), elevated sedimentation rates (averaging in the high 30s) and persistently decreased IgA levels. She was diagnosed as having a lupus/ scleroderma crossover, although the possibility of eosinophilic fascuiitis was considered. (It was ultimately ascertained that she occasionally took Ltroptophan to sleep after long fights.) No disease modifying therapy was given. Supportive diuresis and not steroidal anti-inflammatory agents were prescribed.

Over the following seven years, her ANA rose to 1:1280 (homogeneous) a positive IgG anticardiolipin antibody was found, and her course was complicated by percarditis and supraventrocular tachyarrhythmias. The latter two items were felt to be suggestive of cardiac sclerodrema. Anti RNP was negative and her inflammatory arthritis subsided. CD3 levels. B cell and natural killer cell values do not change. Similar findings have been found in mice in two separate studies. 9.10 Interestingly, the administration of Immunoglobulin production by spleen cells 9 Long-terms hyperbaric oxygen delayed the development of Proteinuria, facial erythema, and lymphadenopathy in an MRI./ 1pr. Mice. Iamoto et al showed that hyperbaric oxygen has immunosuppressive properties modulated by decreasing interluekin 1 and prostaglandin E2 production, but interleukin 6 in production was not altered. 11

How does Hyperbaric Oxygen Affect the Central Nervous System?

Studies of hyperbaric oxygen on the central nervous system show that at tensions of 1.2- 1.5 atmospheres absolute (ATA), it decreases blood flow by 1% to 20%. (Mean of various studies is about 10%.) Two other physiologic changes occur. These include greater permeability of the blood brain barrier to medications and increased oxygen tensions tissues that far outweigh the net effects of mild vasoconstriction. The deformability of erythrocytes is increased resulting in improved transportation in the microvasculature circulation and lactate removal. 12

Hyperbaric oxygen stimulates the metabolism of nerve cells deprived of oxygen. As early as the 1960s, Meijne reported cognitive improvement in patients to performing mathematical calculations and demonstrated increased typewriter skills after hyperbaric oxygen. 13 An area of controversy among Hyperbaricists concerns the possibility that once 1.5 ATA is exceeded, anaerobic metabolism is favored, and thus cognitive results do not improve as well as they would at lower pressures. Di Sabato et al 14 performed a controlled study (with Sham hyperbaric controls) on patients with cluster headaches. The dramatic improvement was attributed to vasoconstriction, decreased edema, increased serotoin synthesis, and decreased cerebral hypoxia. Additionally, in the central nervous system hyperbaric oxygen decreases adrenaline and monoamine oxidase levels as well as promoting axonal regeneration 15.

Hyperbaric Oxygen for Multiple Sclerosis and other autoimmune diseases:As hyperbaric oxygen decreases demyelination from per-vascular edema, more than 6000 patients with multiple sclerosis have undergone this therapy in the past ten years. A published trial by The New England Journal of Medicine suggesting improvement with hyperbaric oxygen in 40 patients in 1983 stimulated considerable interest. 16 However, it was evident that even though hyperbaric oxygen increased helper T lymphocyte levels, patient liked the treatment and reported subjective improvements (especially in the sense of well-being, cognitions and bladder function), four separated placebo-controlled double-blind trials failed to demonstrate any objective benefits of using the Kutz Disability status Scale or any other parameters 17-20 This was also confirmed in a 22 institution multicenter registry 312 patients followed for 2 years. 21 Occasionally patients with other rheumatic syndromes and associated complications have been held to respond to hyperbaric oxygen. Aseptic necrosis complicating system lupus, for example, appears to be worthy of greater scrutiny. Abstracts and presentations at seminars and meetings of hyperbaric oxygen claim benefits for pneumatosis cystoid intestinal in sclerodrema, livedo reticularis with Vasculitis and Raynaud's phenomenon. Articles have appeared advocating hyperbaric oxygen for Crohn's disease and cyclophophadmide-associated hemorrhagic cystitis

How save is hyperbaric oxygen?

Hyperbaric Oxygen is generally quite safe, but serious complications can occur.24 Absolute contraindications to hyperbaric oxygen include pregnancy, underlying malignancy, untreated PNEUMOTHORAX, concomitant therapy with doxorubicin, cis-platinum, or disulfiram. Special considerations need to be taken into account if the patient has upper respiratory tract infections or chronic sinusitis (which make clearing of the ears and sinuses problematic), low seizure thresholds (with high fevers or epilepsy, emphysema with CO2 retention (which suppresses breathing), and congenital spherocytosis (where hempolysis can result).

The most common complication of hyperbaric oxygen is barotrauma to the ears and sinuses caused by pressure changes, which has been reported in about 5% of the cases. Occurring in 0.1- 5% of the patients are hypersensitivity reactions confinement anxiety, central nervous system oxygen toxicity, pulmonary oxygen toxicity and temporary changes in eyesight. To minimize risks, patients are advised to have an ear, nose and throat examination by the treating physician before therapy, not to drink alcohol or take any medication for four hours prior to treatment, and to wear 100% cotton clothing.

Is there a potential role for hyperbaric oxygen in Rheumatic Diseases?

Very little is known about the influence of hyperbaric oxygen on the immune system. Animal models of autoimmune disease and normal mice are conductive to hyperbaric oxygen studies. Hyperbaric oxygen might be useful in combination with other therapeutic modalities. Further study is needed in these areas before proceeding to human trials. Nevertheless, anecdotal testimonials that hyperbaric oxygen helps people think more clearly should be taken seriously and ultimately subjected to a prospective trial. Systemic lupus erthematosus (SLE) is an autoimmune disorder that affects several hundred thousand Americans. Nearly half manifest in similar cognitive deficits that do not respond to CORTICOSTEROIDS. 26 In the past few years, the development of single photon emission computerized tomography (SPECT) has shown hypoperfusion abnormalities bitemporally and bifrontally in patients with SLE and incidentally, with fibromyalgia/chronic fatigue syndromes. 26-29Hyperbaric oxygen is a well-characterized, old technology whose immunodulatory properties and effects on cognition have never been adequately studied. Although relatively expensive, this reasonably safe procedure might have potential heretofore-unrealized applications to the patients with rheumatic disease.

Bojic L., Gosovic S., Kovacecic H., and Denoble P. Hyperbaric Oxygenation in the Treatment of Macular

Degeneration. Split, Yugoslavia: Split Naval Medical Institute, pp. 1-4.

Dr. L. Bojic treated four patients with advanced macular degeneration and severe vision loss in a clinical trail with HBOT. Three of the four patients experienced a doubling of visual acuity after HBOT. The fourth patient experienced a four-fold improvement.Although much more research is needed and HBOT must be considered experimental in this condition, it seems that a trial of 30 90-minute treatments at 1.5 ATA in a monoplace HBO chamber, combined with other therapies such as laser and nutritional supplements, offers hope for additional benefit. This makes good sense, because cells of the retina are specialized neurons actually an extension of the brain. Retinal cells would therefore be expected to respond to HBOT, similarly to brain-injured patients.

http://gizibangka.blogspot.com/PENGERTIAN AUTOIMUNAda beberapa pengertian autoimunitas sebagaimana tercantum dalam kamus kedokteran sebagai berikut : Keadaan penyakit yang ditandai dengan antibodi spesifik atau diperantarai sel respon imun terhadap jaringan tubuh sendiri (autoantigens). Sebuah respon imun yang terjadi salah arah ketika sistem kekebalan tubuh berjalan kacau dan menyerang tubuh sendiri.

Sekitar tahun 1900, Paul Ehrlich, telah menyadari kemungkinan sistem imun dapat menyerang antigen sel tubuh sendiri dan kejadian tersebut dikenal dengan horror autotoxicus yang dapat menimbulkan sejumlah penyakit akut dan kronis, antara lain arthtritis reumatoid, sklerosis multipel, LES dan beberapa jnis DM. Penyakit-penyakit ini secara sederhana ditimbulkan oleh kegagalan imunitas humoral dan atau selular yang tidak dapat membedakan antigen sendiri dari antigen asing Hal tersebut menyerang sel / organ sendiri melalui autoantibodi atau sel T yang self-reaktif. Pada tahun 1959, atas hasil ekperimennya, Jerne, Talmage dan Burnet (1950), maka istilah horror autotoxicus diubah ke dalam teori clonal selection yang merupakan dasar toleransi. Mekanisme proteksi yang kuat diperlukan untuk mencegah terjadinya penyakit autoimun, melindungi individu dari limfosit yang potensial self reaktif terhadap antigen sel tubuh sendiri.

Autoimunitas terdapat pada semua orang sampai batas tertentu. Hal ini biasanya tidak berbahaya dan mungkin fenomena universal hidup vertebrata. Namun, autoimunitas dapat menjadi penyebab dari spektrum yang luas dari penyakit manusia, yang dikenal sebagai penyakit autoimun. Konsep autoimun sebagai penyebab penyakit manusia relatif baru, dan itu tidak diterima ke dalam arus utama pemikiran medis sampai 1950-an dan 1960-an. Penyakit autoimun didefinisikan sebagai penyakit di mana perkembangan dari autoimunitas jinak untuk autoimunitas patogen terjadi. Perkembangan ini ditentukan oleh pengaruh genetik dan lingkungan pemicu. Konsep autoimun sebagai penyebab sebenarnya dari penyakit manusia (bukan konsekuensi atau iringan tidak berbahaya) dapat digunakan untuk menetapkan kriteria yang mendefinisikan suatu penyakit sebagai penyakit autoimun.

Autoimunitas juga dapat didefinisikan sebagai Respon imun terlalu aktif menyebabkan disfungsi imun. Sistem imun gagal untuk memusnahkan dengan tepat antara diri sendiri dan bukan diri sendiri, dan menyerang bagian dari tubuh. Dibawah keadaan sekitar yang normal, banyak sel T dan antibodi bereaksi dengan peptid sendiri. Satu fungsi sel (terletak di thymus dan sumsum tulang) adalah untuk memunculkan limfosit muda dengan antigen sendiri yang diproduksi pada tubuh dan untuk membunuh sel tersebut yang dianggap antigen sendiri, mencegah autoimunitas.

Baru-baru ini telah dihipotesiskan bahwa beberapa protein evolusioner dipertahankan, hadir dalam patogen, organisme komensal dan host mereka, memberikan stimulus yang memulai penyakit autoimun pada individu yang rentan. Mekanisme yang mungkin dari pembentukan autoantigen diduga juga disebabkan oleh meningkatnya splicing non-kanonik yang membuat epitop tak toleran pada antigen. Autoimunitas adalah respons imun terhadap antigen jaringan sendiri yang disebabkan oleh mekanisme normal yang gagal berperan untuk mempertahankan self tolerance sel B, sel T atau keduanya. Autoimunitas melibatkan hilangnya kekebalan tubuh normal sehingga organisme menghasilkan abnormal homeostasis respon terhadap jaringan sendiri. Ciri dari autoimunitas adalah adanya diri-reaktif sel T, autoantibodi, dan peradangan. Contoh menonjol dari penyakit autoimun meliputi: penyakit Celiac, diabetes tipe 1 mellitus, penyakit Addison dan penyakit Graves.

sumber : http://withfriendship.com/images/g/31074/Autoimmunity-picture.gif

Penyakit autoimun adalah kerusakan jaringan atau gangguan fungsi fisiologis yang ditimbulkan oleh respons imun. Oleh karena itu, penyakit autoimun tidak hanya disebabkan kegagalan dalam peranan mempertahankan self-tolerance saja, tetapi juga dapat disebabkan oleh mekanisme lain, seperti infeksi.

TERAPI OKSIGEN HIPERBARIKPENGERTIAN Terapi Oksigen Hiperbarik atau Hiperbaric Oxigen Therapy (HBOT) berasal dari kata hiper berlebih dan barik tekanan Perawatan medis dengan menempatkan pasien dalam ruangan kedap udara pada tekanan yang meningkat hingga 1 sampai 3 kali tekanan atmosfer normal dengan memberikan oksigen murni

PRINSIP-PRINSIP TERAPI Tekanan atmosfir bumi diberikan sekitar 15 pound per inci tekanan di permukaan laut (tekanan satu absolut / ATA = 1) Tekanan 1 ATA adalah 76 mmHg Oksigen yang dihirup secara pernafasan normal adalah sekitar 20% dan nitrogen 80% Pada HBOT, tekanan ditingkatkan hingga 2 ATA pada kondisi oksigen 100% Pasien tidak perlu menggunakan masker atau penutup kepala. Peningkatan tekanan diberikan dikombinasikan dengan peningkatan oksigen hingga 100% murni. Oksigen larut dalam plasma darah dan dalam seluruh sel, jaringan dan cairan sampai 10 kali konsentrasi normal untuk mempertahankan hidup. Peningkatan oksigen hingga 5 kali (20% ke 100%) dan dengan adanya peningkatan 1 ATA dapat menyebabkan peningkatan 10 kali lipat atau 1.000% Konsentrasi oksigen dalam darah dan semua jaringan tubuh lainnya dan cairan tubuh dapat mencapai 20 kali konsentrasi normal

MEKANISME TERAPI Meningkatkan konsentrasi oksigen di semua jaringan tubuh, bahkan pada kondisi aliran darah berkurang atau tersumbat Merangsang pertumbuhan pembuluh darah baru ke lokasi dengan sirkulasi berkurang, meningkatkan aliran darah ke daerah yang mengalami penyumbatan arteri Menyebabkan dilatasi arteri rebound setelah HBOT, sehingga diameter pembuluh darah meningkat lebih besar daripada ketika terapi dimulai, memperbaiki aliran darah ke organ. Peningkatan tekanan oksigen parsial yang dicapai jauh lebih tinggi dari pernafasan monobaric (pernafasan pada tekanan normal) menyebabkan kapasitas transpor oksigen darah. Pada monobaric, transpor oksigen dibatas oleh kapasitas oksigen yang diikat hemoglobin dalam sel darah merah dan sangat sedikit oksigen yang diangkut oleh plasma darah. Pada HBOT, oksigen yang diangkut plasma darah meningkat secara signifikan. Pengobatan dimulai dengan pasien masuk ke dalam kamar dan pintu ditutup, oksigen mulai beredar. Ini dilakukan secara bertahap dalam tekanan yang juga ditingkatkan dan disebut kompresi Tingkat kompresi disesuaikan dengan toleransi pasien, dengan mungkin timbul sensasi kehangatan yang bersifat sementara dan rasa penuh di telinga. Kompresi dilakukan selama 10 15 menit tergantung kemampuan pasien untuk menyesuaikan tekanan, sehingga sensasi penuh di telinga dapat diatasi Bila pasien telah dapat menyesuaikan diri, maka pasien dapat beristirahat atau beraktifitas dalam ruangan pada suhu kamar selama 1 jam. Pada akhir pengobatan, tekanan dikurangi secara bertahap (dekompresi) yang umumnya juga berlangsung 10 15 menitINDIKASI Komite Pengobatan Bawah Laut dan Hiperbarik Amerika Serikat merekomendasikan pengobatan : Penyakit dekompresi Emboli gas arteri Keracunan CO dengan/tanpa keracunan sianida Radiasi tertunda cedera jaringan lunak Gangrene (infeksi serius) Infeksi jaringan lunak dimana jaringan mati (nekrotik) Kehilangan darah yang parah (anemia) pada saat transfusi tidak ada pilihan Luka bakar termal Abses di kepala atau otak Osteomiielitis (radang tulang kronis) yang tidak merespon pengobatan standar Penyumbatan arteri retinaKEMUNGKINAN KOMPLIKASI DAN MASALAH Risiko yang terjadi mirip dengan gangguan menyelam. Perubahan tekanan menyebabkan menekan atau barotrauma di jaringan sekitar udara yang terjebak di dalam tubuh, seperti paru-paru, di belakang gendang telinga, di dalam sinus paranasal, atau terperangkap di gusi. Dapat juga menyebabkan keracunan oksigen, pandangan yang menjadi kabur sementara yang disebabkan pembengkakan lensa Kemungkinan terjadinya kebakaranKONTRA INDIKASI Kontraindikasi absolut : pneumotoraks yang tidak terobati Pasien yang mengkonsumsi obat kemoterapi : doksorubisin (adriamycin) dan cisplatin; disulfiram (antabuse) untuk pengobatan alkoholisme dan mafenide asetat (sulfamylon) untuk menekan infeksi bakteri pada luka bakar Kontra indikasi relatif : ISPA (dapat menekan sinus di hidung dan telinga) Demam tinggi Emfisema dengan retensi CO2 yang dapat menyebabkan pneumotoraks Riwayat operasi toraks Penyakit ganas : kanker Telinga bagian tengah (kemungkinan barotrauma) kehamilan

http://www.medicinenet.com/scleroderma/article.htmScleroderma facts Scleroderma is a disease of the connective tissue featuring skin thickening, that can involve scarring, blood vessel problems, varying degrees of inflammation, and is associated with an overactive immune system. Scleroderma is classified into localized scleroderma and systemic sclerosis. CREST syndrome is a limited form of systemic sclerosis. Patients with scleroderma can have specific antibodies (ANA, anticentromere or antitopoisomerase) in their blood which suggest autoimmunity. Treatment of scleroderma is directed toward the individual's symptom(s) that is(are) most debilitating.What is scleroderma?Scleroderma is an autoimmune disease of the connective tissue featuring skin thickening, spontaneous scarring, blood vessel disease, varying degrees of inflammation, associated with an overactive immune system. Autoimmune diseases are illnesses that occur when the body's tissues are attacked by its own immune system. Scleroderma is characterized by the formation of scar tissue (fibrosis) in the skin and organs of the body. This leads to thickness and firmness of involved areas. Scleroderma, when it's diffuse or widespread over the body, is also referred to as systemic sclerosis.What causes scleroderma?The cause of scleroderma is not known. Researchers have found some evidence that certain genes are important hereditary factors, but the environment seems to also play a role. The result is activation of the immune system in a susceptible individual, causing injury to tissues that result in injury similar toscar-tissue formation. The fact that genes seem to cause a predisposition to developing scleroderma means that inheritance at least plays a partial role. It is not unusual to find other autoimmune diseases in families of scleroderma patients. Some evidence for the role genes may play in leading to the development of scleroderma comes from the study of Choctaw Native Americans who are the group with the highest reported prevalence of the disease. The disease is more frequent in females than in males.What are risk factors for developing scleroderma?Because of the known association of certain genes with scleroderma, it is felt that unclear combinations of exposures to environmental factors and possibly certain viruses may trigger the development of scleroderma in genetically susceptible people.How is scleroderma classified?Scleroderma can be classified in terms of the degree and location of the skin and organ involvement. Accordingly, scleroderma has been categorized into two major groups, localized scleroderma and systemic sclerosis. Systemic sclerosis is further subdivided into either diffuse or limited forms.Localized scleroderma skin changes are in isolated areas, either as morphea patches or linear scleroderma. Morphea is scleroderma that is localized to a patchy area of the skin that becomes hardened and slightly pigmented. Sometimes morphea can cause multiple lesions in the skin. Morphea is not associated with disease elsewhere in the body. Linear scleroderma is scleroderma that is localized usually to a lower extremity, frequently presenting as a strip of hardening skin down the leg of a child. Linear scleroderma in children can stunt bone growth of the affected limb. Sometimes linear scleroderma is associated with a "satellite" area of a patch of localized scleroderma skin, such as on the abdomen.The diffuse form of scleroderma (diffuse systemic sclerosis) involves symmetric thickening of skin of the extremities, face, and trunk (chest, back, abdomen, or flanks) that can rapidly progress to hardening after an early inflammatory phase. Organ disease can occur early on and be serious and significantly decrease life expectancy. Organs affected include the esophagus, bowels, scarring (fibrosis) of the lungs, heart, and kidneys. High blood pressure can be a troublesome side effect and can lead to kidney failure (renal crisis).The limited form of scleroderma tends to have far less skin involvement with skin thickening confined to the skin of the fingers and face. The skin changes and other features of disease tend to occur more slowly than in the diffuse form. Because a characteristic clinical pattern can occur in patients with the limited form of scleroderma, this form has taken another name that is composed of the first initials of the common components. Thus, this form is also called the "CREST" variant of scleroderma. CREST represents the following features:C...Calcinosisrefers to the formation of tiny deposits of calcium in the skin. This is seen as hard, whitish areas in the superficial skin, commonly overlying the elbows, knees, or fingers. These firm deposits can be tender, can become infected, and can fall off spontaneously or require surgical removal. This is the least common of the CREST scleroderma variant features.R...Raynaud's phenomenonrefers to the spasm of the tiny artery vessels supplying blood to the fingers, toes, nose, tongue, or ears. These areas turns blue, white, then red after exposure to extremes of cold, or even sometimes with extremes of heat or emotional upset. This can lead to tiny areas of damage to the tips of the fingers (digital ulcers) or larger areas of dead skin on the ends of the fingers.E...Esophagus disease in scleroderma is characterized by poorly functioning muscle of the lower two-thirds of the esophagus (the swallowing tube through which food passes from the mouth to the stomach). This can lead to an abnormally wide esophagus that allows stomach acid to backflow into the esophagus to cause heartburn, inflammation, and potentially scarring that narrows the esophagus. This can eventually lead to difficulty in passing food from the mouth through the esophagus into the stomach. Symptoms of heartburn are treated aggressively in patients with scleroderma in order to prevent injury to the esophagus.S...Sclerodactylyis the localized thickening and tightness of the skin of the fingers or toes. This can give them a "shiny" and slightly puffy appearance. The tightness can cause severe limitation of motion of the fingers and toes. These skin changes generally progress much slower that those of patients with the diffuse form of scleroderma.T...Telangiectasias are tiny red areas, frequently on the face, hands, and in the mouth behind the lips. These areas blanch when they are pressed upon and represent widened (dilated) capillaries.Patients with limited systemic sclerosis can have variations of CREST with differing manifestations, for example, CRST, REST, ST, etc. Patients can also have "overlap" illness with features of both CREST and the diffuse form of scleroderma. Some patients have overlaps of scleroderma and other connective tissue diseases, such as rheumatoid arthritis, systemic lupus erythematosus, and polymyositis. When features of scleroderma are present along with features of polymyositis, systemic lupus erythematosus, and certain abnormal blood tests the condition is referred to as mixed connective tissue disease (MCTD).What are scleroderma symptoms and signs?The symptoms of scleroderma depend on the type of scleroderma present and the extent of external and internal involvement in the individual affected. Because scleroderma can affect the skin, esophagus, blood vessels, kidneys, lungs, blood pressure and bowels, the symptoms it causes can involve many areas of the body.Scleroderma affects the skin to cause local or widespread signs of inflammation (redness, swelling, tenderness,itching, and pain) that can lead to skin tightness or hardening. These skin changes can be widespread, but it's most common for them to affect the fingers, feet, face, and neck. This can lead to decreased range of motion of the fingers, toes, and jaw. Tiny areas of calcification (calcinosis), while not common, can sometimes be noticed as hard nodules at the tips of the elbows or in the fingers.Scleroderma affecting the esophagus leads to heartburn. This is directly a result of stomach acid flowing back up into the esophagus. Sometimes this can lead to scarring of the esophagus, resulting in narrowing with difficulty swallowing food and/or localized pain in the central chest.Blood vessels that can be affected include the tiny arterioles of the finger tips, toes, and elsewhere. These vessels can have a tendency to spasm when the areas are exposed to cold, leading to blueness, whiteness, and redness of involved fingers, toes, and sometimes nose or ears. These color changes are referred to asRaynaud's phenomenon. Raynaud's phenomenon can cause inadequate supply of oxygen to the involve tips of fingers or toes, causing tiny ulcers or blackened (dead) skin. Sometimes Raynaud's phenomenon is also associated with tingling. Other blood vessels that can be involved in scleroderma are the tiny capillaries of the face, lips, mouth, or fingers. These capillaries widen (dilate), forming tiny, red blanching spots, called telangiectasias.Elevated blood pressure is potentially serious and can lead to kidney damage (renal crisis). Symptoms includeheadache, fatigue, and in severe cases,stroke. Blood pressure monitoring and control is essential.Inflammation of the lungs in scleroderma can cause scarring, resulting inshortness of breath, especially with physical exertion. Elevated pressure in the arteries to the lungs (pulmonary hypertension) can also cause shortness of breath and difficulty getting an adequate breath with activity.Scleroderma affecting the large bowel (colon) most often causesconstipationbut can also lead to cramping anddiarrhea. When this is severe, complete stool blockage (fecal impaction) can result.How is scleroderma diagnosed?The diagnosis of the scleroderma syndrome is based on the finding of the clinical features of the illnesses. In addition, nearly all patients with scleroderma have blood tests that suggest autoimmunity, because antinuclear antibodies (ANAs) are usually detectable. A particular antibody, the anticentromere antibody, is found almost exclusively in the limited, or CREST, form of systemic sclerosis. Anti-Scl 70 antibody (antitopoisomerase I antibody) is most often seen in patients with the diffuse form of systemic sclerosis.Other tests are used to evaluate the presence or extent of any internal disease. These may include upper and lower gastrointestinal tests to evaluate the bowels,chest X-rays, lung-function testing (pulmonary function test), andCAT scanningto examine the lungs,EKGandechocardiograms, and sometimes heart catheterization to evaluate the pressure in the arteries of the heart and lungs.What is the treatment for scleroderma?Treatment of scleroderma is directed toward the individual feature(s) affecting different areas of the body.Aggressive treatments of elevations in blood pressure have been extremely important in preventingkidney failure. Blood-pressure medications, particularly the angiotensin converting enzyme (ACE) inhibitor class of drugs, such ascaptopril(Capoten), are frequently used.Some research indicates thatcolchicinecan be helpful in decreasing the inflammation and tenderness that periodically accompanies the calcinosis nodules in the skin. Skinitchingcan be relieved with lotions (emollients) such as Eucerin, Lubriderm, and Bag Balm.Mild Raynaud's phenomenon may require only hand warming and protection. Low-dose aspirin is often added to prevent tinyblood clotsin the fingers, especially in patients with a history of fingertip ulcerations. Moderate Raynaud's phenomenon can be helped by medications that open up the arteries, such asnifedipine(Procardia, Adalat),nicardipine(Cardene), and diltiazem (Cardizem), or with topicalnitroglycerinapplied to the most affected digit (most effective on the sides of the digit where the arteries are). Gently applied finger splinting can protect tender tissues. (It is important to not constrict the tiny arteries on the sides of the fingers when protecting them with splints, braces, or band-aid materials.) A class of medications that is typically used fordepression, called serotonin reuptake inhibitors, such asfluoxetine(Prozac), can sometimes improve the circulation of the affected digit. Drugs that constrict blood vessels, such as pseudoephedrine (Sudafed decongestant) should be avoided. Severe Raynaud's phenomenon can require surgical procedures, such as those to interrupt the nerves of the finger that stimulate constriction of the blood vessels (digital sympathectomy). Ulcerations of the fingers can require topical or oral antibiotics.Esophagus irritation and heartburn can be relieved withomeprazole(Prilosec),esomeprazole(Nexium), orlansoprazole(Prevacid). Antacids can also be helpful. Elevating the head of the bed can reduce the back-flow of acid into the esophagus that causes inflammation and heartburn. Avoidingcaffeineandcigarette smokingalso helps. Of note, there is an increased risk of developing lung cancer in persons with scleroderma. This risk is even greater in those who smoke.Constipation, cramping, anddiarrheais sometimes caused by bacteria that can be treated withtetracyclineorerythromycin. Studies have shown that erythromycin could also be used. Increased fluid intake andfiberintake are good general measures.Irritated, itchydry skincan be helped by emollients such as Lubriderm, Eucerin, Bag Balm histamine 2 blockers, ortrazodone(Desyrel).Telangiectasias, such as those on the face, can be treated with local laser therapy. Sun exposure should be minimized as it can worsen telangiectasias.Approximately 10% of patients with the CREST variant develop elevated pressures in the blood vessels to the lungs (pulmonary hypertension). Abnormally elevated blood pressure of the arteries supplying the lungs is often treated with calcium antagonist medications, such asnifedipine(Procardia), and blood-thinning drugs (anticoagulation). More severepulmonary hypertensioncan be helped by continuous intravenous infusion or inhalation of prostacyclin (Iloprost). Taken by mouth,bosentan(Tracleer) is now also available to treat pulmonary hypertension. In addition,sildenafil(Revatio) andtadalafil(Cialis) have been FDA approved to treat pulmonary hypertension.Additionally, medications are used to suppress the overly active immune system that seems to be spontaneously causing the disease in organs. Medications used for this purpose includepenicillamine,azathioprine(Imuran, Azasan), andmethotrexate(Rheumatrex, Trexall). Recent research has found that low-dose penicillamine (Depen, Cuprimine) (125 mg every other day) is as effective as previously used high doses of penicillamine, with less toxicity. Serious inflammation of the lungs (alveolitis) can require immune suppression withcyclophosphamide(Cytoxan) along withprednisone(Deltasone, Liquid Pred). The optimal treatment of scleroderma lung disease is an area of active research. Stem-cell transplantation is being explored as a possible option.No medication has been found to be universally effective for all patients with scleroderma. In an individual patient, the illness may be mild and not require treatments. In some, the disease is ravaging, relentless, and can lead to death.What is the prognosis (outlook) for patients with scleroderma?A patient's prognosis is optimized with close monitoring of overall health status and treatment of complications, especially elevated blood pressure. Research indicates that the critical period of organ risk is generally within the first three years of skin involvement. This means that patients can be reassured that their risk of organ-threatening complications is significantly less after three years of having skin symptoms.Much more research is needed in all areas of scleroderma disease, from cause to treatment. Today scleroderma continues to challenge medical scientists. Researchers are evaluating the effectiveness ofthalidomide(Thalomid) for the treatment of scleroderma. More sensitive tests to detect early lung disease of scleroderma are also being evaluated. Psoralen and ultraviolet light therapy (PUVA) is being studied as a possible treatment for limited scleroderma.Many researchers are investigating the roles of various cell messengers, called cytokines, in causing scleroderma. Researchers are also currently studying a hormone ofpregnancy, calledrelaxin, for the treatment of scleroderma. Preliminary results suggest that it may improve scleroderma. Relaxin normally loosens the ligaments of the pelvis and ripens the womb for childbirth. How it might work in scleroderma is unclear.It is clear that our understanding of the effects of the immune system in scleroderma is greatly improving. A vast number ofclinical research trialsare under way that are evaluating potential treatments for various aspects of the disease to improve the prognosis for patients with scleroderma.Can scleroderma be prevented?There is no prevention method or diet to avoid or decrease the risk of scleroderma.REFERENCES:

Jimenez, Sergio A., and Patrick M. Cronin. "Scleroderma." eMedicine.com. Jan. 5, 2010. .

Koopman, William, et al., eds.Clinical Primer of Rheumatology. Philadelphia: Lippincott Williams & Wilkins, 2003.

Ruddy, Shaun, et al., eds.Kelley's Textbook of Rheumatology. Philadelphia: W.B. Saunders Co., 2000.

http://www.merckmanuals.com/home/bone_joint_and_muscle_disorders/autoimmune_disorders_of_connective_tissue/systemic_sclerosis_scleroderma.htmlSystemic Sclerosis (Scleroderma)Share This

Systemic sclerosis (scleroderma) is a rare, chronic disorder characterized by degenerative changes and scarring in the skin, joints, and internal organs and by blood vessel abnormalities. Swelling of the fingers, intermittent coolness and blue discoloration of the fingers, joints freezing in permanent (usually flexed) positions (contractures), and damage to the gastrointestinal system, lungs, heart, or kidneys may develop. People often have antibodies in the blood characteristic of an autoimmune disorder. No treatment changes the course of the disorder. Symptoms and organ dysfunction are treated.The cause of systemic sclerosis is not known. The disorder is 4 times more common among women than men and is rare among children. Symptoms of systemic sclerosis may occur as part of mixed connective tissue disease, and some people with mixed connective tissue disease develop severe systemic sclerosis. Systemic sclerosis can occur in limited forms, for example, sometimes affecting just the skin or mainly only certain parts of the skin or as CREST syndrome. However, systemic sclerosis often causes damage that is widespread throughout the body (called diffuse or generalized systemic sclerosis).SymptomsThe usual initial symptom of systemic sclerosis is swelling, then thickening and tightening of the skin at the ends of the fingers. Raynaud's syndrome, in which the fingers suddenly and temporarily become very pale and tingle or become numb, painful, or both in response to cold or emotional upset (seePeripheral Arterial Disease: Raynaud's Syndrome), is also common. Fingers may become bluish. Heartburn, difficulty in swallowing, and shortness of breath are occasionally the first symptoms of systemic sclerosis. Aches and pains in several joints often accompany early symptoms. Sometimes inflammation of the muscles (polymyositis), with its accompanying muscle pain and weakness, develops.Skin Changes:Systemic sclerosis can damage large areas of skin or only the fingers (sclerodactyly). Sometimes systemic sclerosis tends to stay restricted to the skin of the hands. Other times, the disorder progresses. The skin becomes more widely taut, shiny, and darker than usual. The skin on the face tightens, sometimes resulting in an inability to change facial expressions. Sometimes dilated blood vessels (telangiectasia often referred to as spider veins) can appear on the fingers, chest, face, lips, and tongue, and bumps composed of calcium can develop on the fingers, on other bony areas, or at the joints. Sores can develop on the fingertips and knuckles.Scleroderma

Joint Changes:Sometimes, a grating sound can be felt or heard as inflamed tissues move over each other, particularly at and below the knees and at the elbows and wrists. The fingers, wrists, and elbows may become stuck (forming a contracture) in flexed positions because of scarring in the skin.Gastrointestinal System Changes:Scarring commonly damages the lower end of the esophagus (the tube connecting the mouth and stomach). The damaged esophagus can no longer propel food to the stomach efficiently. Swallowing difficulties and heartburn eventually develop in many people who have systemic sclerosis. Abnormal cell growth in the esophagus (Barrett's esophagusseeTumors of the Digestive System: Risk Factors) occurs in about 33% of the people, increasing their risk of esophageal blockage (stricture) due to a fibrous band or their risk of esophageal cancer. Damage to the intestines can interfere with food absorption (malabsorption) and cause weight loss.Lung and Heart Changes:Systemic sclerosis can cause scar tissue to accumulate in the lungs, resulting in abnormal shortness of breath during exercise. The blood vessels that supply the lungs can be affected (their walls thicken), so they cannot carry as much blood. Therefore blood pressure within the arteries that supply the lungs can increase (a condition called pulmonary hypertensionseePulmonary Hypertension). Systemic sclerosis can also cause several life-threatening heart abnormalities, including heart failure and abnormal rhythms.Kidney Changes:Severe kidney disease can result from systemic sclerosis. The first symptom of kidney damage may be an abrupt, progressive rise in blood pressure. High blood pressure is an ominous sign, although treatment usually controls it.CREST Syndrome:CREST syndrome, also called limited cutaneous systemic sclerosis (sclerosis) is usually a less severe form of the disorder that is less likely to cause serious internal organ damage. It is named for its symptoms:Calcium deposits in the skin and throughout the body,Raynaud's syndrome,Esophageal dysfunction,Sclerodactyly (skin damage on the fingers), andTelangiectasia (dilated blood vessels or spider veins). Skin damage is limited to the fingers. People who have CREST syndrome can develop pulmonary hypertension, which can cause heart and lung failure. The drainage system from the liver may become blocked by scar tissue (biliary cirrhosis), resulting in liver damage and jaundice.DiagnosisA doctor diagnoses systemic sclerosis by the characteristic changes in the skin and internal organs. The symptoms may overlap with those of several other disorders, but the whole pattern is usually distinctive. Laboratory tests alone cannot identify systemic sclerosis because test results, like the symptoms, vary greatly. However, antinuclear antibodies are present in the blood of more than 90% of people with systemic sclerosis. An antibody to centromeres (part of a chromosome) is often present in people who have CREST syndrome. A different antibody (called anti-topoisomerase) is often present in people with the more diffuse generalized form.PrognosisSometimes systemic sclerosis worsens rapidly and becomes fatal. At other times, it affects only the skin for decades before affecting internal organs, although some damage to internal organs (such as the esophagus) is almost inevitable, even in CREST syndrome. The course is unpredictable. Overall, about 65% of people live for at least 10 years after the diagnosis is made. The prognosis is worst for those who have heart, lung, or, particularly, kidney damage.TreatmentNo drug can stop the progression of systemic sclerosis. However, drugs can relieve some symptoms and reduce organ damage. Nonsteroidal anti-inflammatory drugs (NSAIDsseePain: Nonsteroidal Anti-Inflammatory Drugs) help relieve joint pain. If the person has weakness because of polymyositis, corticosteroids may be needed. Drugs that suppress the immune system, such ascyclophosphamide

andazathioprine

, may help some people whose lungs are affected. Doctors treat severe pulmonary hypertension with the drugsbosentan

orepoprostenol

. The person may also be given anticoagulants.Heartburn can be relieved by eating small meals, taking antacids, and using proton pump inhibitors, which block stomach acid production. Sleeping with the head of the bed elevated often helps. Areas of the esophagus narrowed by scar tissue can be surgically widened (dilated).Tetracycline

or other antibiotics can help prevent malabsorption of food caused by excessive growth (overgrowth) of bacteria in the damaged intestine. A calcium channel blocker (such asnifedipine

) may relieve the symptoms of Raynaud's syndrome (seePeripheral Arterial Disease: Raynaud's Syndrome) but may also increase the reflux of stomach acid. Drugs for high blood pressure, particularly angiotensin-converting enzyme (ACE) inhibitors, are useful in treating kidney disease and the rise in blood pressure.Physical therapy and exercise can help to maintain muscle strength but cannot totally prevent joints from freezing in contractures.